ReviewToxins2020
Molecular and Cellular Mechanisms that Induce Arterial Calcification by Indoxyl Sulfate and P-Cresyl Sulfate.
Review in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 62 citations in OpenAlex.
- Cardiovascular-kidney-metabolic syndrome through the lens of gut‑derived uremic toxins.Gut microbes · 2026Review
- Chronic kidney disease-associated pruritus: a perspective on skin barrier damage.Renal failure · 2026Review
- Indoxyl Sulfate, Cardiac Biomarkers, and Left Ventricular Wall Thickening in Cats with Chronic Kidney Disease.Veterinary sciences · 2026Article
- Article
- Review
- Gut-Derived Uremic Toxins as a Risk Factor for Vascular Damage in Patients with Chronic Kidney Disease.International journal of molecular sciences · 2026Observational
- Nutritional Modulation of the Gut-Kidney Axis.Nutrients · 2026Review
- Gut-Kidney Axis: Unraveling the Role of the Microbiome in Chronic Kidney Disease.Biomedicines · 2026Review
- Raman signatures ofFrontiers in microbiology · 2026Article
- Effects of conventional yogurt, probiotic-enriched yogurt, and isolated probiotic on bone and heart parameters in a chronic kidney disease experimental model.European journal of nutrition · 2025Article
- Calciphylaxis diagnosis, management and future directions: a comprehensive update on behalf of the European Renal Association CKD-MBD Working Group.Clinical kidney journal · 2025Review
- Lymphocyte Phenotypes and Protein-Bound Uremic Toxins as Determinants of Clinical Outcomes in Hemodialysis Patients.International journal of molecular sciences · 2025Observational
- Vascular Smooth Muscle Cell Metabolic Reprogramming in Arteriovenous Fistula Failure.Biomedicines · 2025Review
- Serum Indoxyl Sulfate as a Potential Biomarker of Aortic Stiffness in Persons with Type 2 Diabetes Mellitus.Medicina (Kaunas, Lithuania) · 2025Article
- Gamma-tocopherol vitamin E enhances the cytotoxicity of p-cresyl sulfate to renal tubular cells.European journal of medical research · 2025Article
- SerumLife (Basel, Switzerland) · 2025Article
- Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Serum midkine level and its association with subclinical coronary artery calcification and carotid atherosclerosis in chronic kidney disease.BMC nephrology · 2025Article
- UnravelingFrontiers in pharmacology · 2025Review
- The Gut-Kidney Axis in Chronic Kidney Diseases.Diagnostics (Basel, Switzerland) · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protein-bound uremic toxins, indoxyl sulfate (IS) and p-cresyl sulfate (PCS), are considered to be harmful vascular toxins. Arterial media calcification, or the deposition of calcium phosphate crystals in the arteries, contributes significantly to cardiovascular complications, including left ventricular hypertrophy, hypertension, and impaired coronary perfusion in the elderly and patients with chronic kidney disease (CKD) and diabetes. Recently, we reported that both IS and PCS trigger moderate to severe calcification in the aorta and peripheral vessels of CKD rats. This review describes the molecular and cellular mechanisms by which these uremic toxins induce arterial media calcification. A complex interplay between inflammation, coagulation, and lipid metabolism pathways, influenced by epigenetic factors, is crucial in IS/PCS-induced arterial media calcification. High levels of glucose are linked to these events, suggesting that a good balance between glucose and lipid levels might be important. On the cellular level, effects on endothelial cells, which act as the primary sensors of circulating pathological triggers, might be as important as those on vascular smooth muscle cells. Endothelial dysfunction, provoked by IS and PCS triggered oxidative stress, may be considered a key event in the onset and development of arterial media calcification. In this review a number of important outstanding questions such as the role of miRNA's, phenotypic switching of both endothelial and vascular smooth muscle cells and new types of programmed cell death in arterial media calcification related to protein-bound uremic toxins are put forward and discussed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.